Coxsackievirus B3 (CVB3) infection of AJ, B10.A, CSS3 and B6.chr3AJ (heart tissue day 4)

The pathogenesis of viral myocarditis is a multifactorial process involving host genetics, viral genetics and the environment in which they interact. Here, we used a model of infection with Coxsackievirus B3 to characterize the contribution of host genetics to viral myocarditis. We determined heart CVB3 load in mice from a classical intercross between progenitors A/J (H2a) and B10.A-H2a (B10.A) of different genetic backgrounds but with a common H2 haplotype. Here we compare whole genome expression patterns in infected and uninfected A/J and B10.A mice in order to determine which gene expression programs are common or distinct to each strain. Total RNA obtained from hearts of 3 AJ, 3 B10.A(H2a), 3 CSS3 and 3 B6.chr3AJ that were infected or uninfected with CVB3(CG) at 400pfu/g and collected at day 4 post infection.

病毒性心肌炎的发病机制为多因素过程，涉及宿主遗传学、病毒遗传学以及二者相互作用的环境条件。本研究采用柯萨奇病毒B3（Coxsackievirus B3, CVB3）感染模型，解析宿主遗传学在病毒性心肌炎发生中的贡献。我们对遗传背景存在差异但共享同一H2单倍型（H2 haplotype）的亲本A/J（H2a）与B10.A-H2a（B10.A）进行经典互交，对其后代开展心脏CVB3载量测定。为明确各品系共有的或特异性的基因表达程序，我们对比了感染与未感染状态下A/J及B10.A小鼠的全基因组表达谱。本研究从3只A/J、3只B10.A(H2a)、3只CSS3及3只B6.chr3AJ小鼠的心脏组织中提取总RNA，这些小鼠均以400噬斑形成单位（plaque-forming unit, pfu）/克的剂量感染CVB3（CG株）或不予感染，并于感染后第4天采集样本。